2. Endodontic
• Branch of dentistry
concerned with the
morphology, physiology
and pathology of the
human dental pulp and
periradicular tissues.
3. Endodontic
• Its study and practice include the
biology of the normal pulp tissue.
• The etiology, diagnosis, prevention
and treatment of diseases and
injuries of the pulp and associate
periradicular conditions.
4. Dental Pulp
• A richly vascularized and
innervated specialized connective
tissue of ectomesenchymal
origin.
• Contained in the central space of
a tooth, surrounded by the
dentin, with
inductive, formative, nutritive, se
nsory and protective functions.
5. Dental Pulp
• The pulp has essentially no
collateral circulation.
• Its main function is dentin
deposition during tooth
formation .
• Odontoblasts, the dentin-
forming cells.
9. Causes of Pulpal Injury
• Bacterial
▫ Products of bacterial
metabolism are the major
cause of pulpal injury.
10. Pathways of Pulpal Infection
Dental caries
• Is the most common
pathway for microbes
to enter the root canal
system.
• Most common cause
of pulp disease
▫ Bacteria and their by
products may have an
effect on the pulp
before direct exposure
11. Reaction to Caries
• Decrease in the permeability of
the dentin
• The most common response to
caries is dentin sclerosis.
• Formation of new dentin
• Inflammatory reactions.
12. Microorganisms Associated with
Endodontic Disease
• Primary root canal infections are
polymicrobial, typically dominated by obligate
anaerobic bacteria.
• In infected root canals a selective process takes
place over time that allows anaerobic bacteria to
predominate.
▫ Apparently tissue fluid, necrotic pulp tissue, low-
oxygen tension, and bacteria by products determine
which bacteria will predominate.
• E. Faecalis has been isolated from cases of failing
RCT.
13. Diagnosis Sequence
• Systematic approach
• Obtain pertinent information
▫ medical history
▫ dental history
• Ask about patient’s pain history (subjective)
▫ location
▫ duration
▫ severity
▫ character
▫ eliciting stimuli
• Interpret data gathered.
• Formulate a differential diagnosis.
• Formulate a final diagnosis.
14. PAIN
Source
Internally: pulpal
Externally
Quality
Sharp
Related to Aδ fibers
Typical of acute tissue injury
Dull, boring or throbbing
Related to severe damage to tissues
C fibers respond
15. PAIN
May arise in the periodontal ligament.
▫ Tooth will be sensitive to
percussion, chewing, and possibly palpation.
▫ Possible causes:
Pulpal origin - the periodontitis is caused by an
extension of pulpal disease
In these cases the pulp is unresponsive to pulp
testing, so pulpal vitality testing is key to the
diagnosis.
Periodontal origin
Occlusion
16. PAIN
• Intensity of the Pain
▫ Described in a scale of 0 to 10 where 0 = no pain and
10 = most painful.
▫ Pulpal pain produced by Aδ fibers can be
excruciating and often approaches the upper limits of
the scale.
▫ Severe pain is rarely encountered in periodontal
disorders.
▫ Mild to moderate pain can be found in either pulpal
or periodontal pathosis.
▫ Acute pain is usually a reliable sign that the pain is of
pulpal origin.
17. PAIN
• The ability of the patient to locate the offending
tooth depends if the inflammatory state is limited to
the pulp tissue.
▫ Pulp contains no proprioceptive fibers.
• If the inflammatory process extends beyond the
apical foramen and affects the periodontal ligament
it will be easier for the patient to identify the source
of the pain.
• Dental referred pain
▫ Pain from a diseased pulp could be referred to
adjacent teeth or teeth in the opposing quadrant.
▫ Most commonly related to irreversible pulpitis
18. Diagnosis Sequence
• Extra oral and Intra oral Examination
Facial swelling
Facial asymmetries
Bimanual palpation
Detection of tender lymph nodes
19. Diagnosis Sequence
• Extra oral and Intra oral Examination
Presence of defective
restorations
Discolored crowns
Recurrent caries
Fractures
20. Intraoral Examination
• Soft Tissues
▫ Any tissue to be examined must be dried.
▫ Unusual alterations of color, texture, consistency or
contour of soft tissues.
Examine for sinus tracts, redness or swelling.
Sinus tract = passageway from an enclosed
area of infection to an epithelial surface
Fistula = abnormal link between two natural
body cavities or two internal organs
Parulis = hyperplasic tissue at gingival
opening or sinus tract
21. Intraoral Examination
• Hard tissues
Search for signs of caries
Tooth discolorations
Abrasions, attritions and
erosions
Fractured teeth
Restorations: appropriate or
defective?
Developmental defects
Pulp polyps
22. Intraoral Examination
• Hard tissues
Search for signs of caries
Tooth discolorations
Abrasions, attritions and
erosions
Fractured teeth
Restorations: appropriate or
defective?
Developmental defects
Pulp polyps
23. Intraoral Examination
• Hard tissues
Search for signs of caries
Tooth discolorations
Abrasions, attritions and
erosions
Fractured teeth
Restorations: appropriate or
defective?
Developmental defects
Pulp polyps
24. Diagnosis Sequence
• Radiographic examination
▫ Radiographs are helpful but have
limitations.
▫ There is a tendency to over-rely on
radiographs often with unfortunate
consequences.
▫ Periapical
▫ Bite-wings are usually necessary
25. Radiographic Interpretation
• Causes of pulpitis
• Stage of root development
• Calcification of canals
• Pulp stones
26. Radiographic Interpretation
• Causes of pulpitis
• Stage of root development
• Calcification of canals
• Pulp stones
27. Radiographic Interpretation
• Size, shape, number and
curvature of roots.
• Number, direction, width (M-
D) of the canals and pulp
chamber
▫ Sudden changes in
appearance from dark to light
indicate bifurcation.
▫ Presence of extra roots or
canals should always be
suspected.
30. Radiographic Interpretation
• Apical Radiolucencies
▫ Significant medullar bone
destruction may occur before
any radiographic signs begin to
appear.
▫ To be able to see radiographic
changes, the inflammatory
process should have begun to
demineralize the cortical plate.
31. Radiographic Interpretation
A change in the x-ray beam angle
can show missing roots/ canals
A bitewing shows decay not
shown in the periapical x-ray
32. Diagnosis Sequence
• The best test is to repeat the stimulus
that reportedly causes the pain to
identify the offending tooth.
• Thermal tests
• Percussion and palpation sensitivity
tests to determine periapical status
Palpation over the apex
Digital pressure on tooth if severed pain upon
mastication is reported
Light percussion with the mirror’s handle
Selective biting on an object
• Periodontal examination
Always necessary
33. Palpation
• Digital pressure to check
tenderness in the oral tissue
underlying suspected teeth
• Indicates how far the
inflammatory process has
extended periapically.
• May detect incipient
swelling.
• A positive response indicates
that the underlying tissues
are inflamed.
34. Percussion
• Indicates some degree of
inflammation in the
periodontal ligament.
• It is not a test of pulp vitality.
▫ Occlusion
▫ Trauma
▫ Sinusitis
▫ Periodontal Disease
▫ Crack tooth
▫ Extension of pulpal disease
into the PDL
35. Mobility
• Provides an indication
of the integrity of the
attachment apparatus.
36. Mobility
• Causes:
▫ Periodontal disease
▫ Root fracture
▫ Recent trauma
▫ Chronic bruxism
▫ Orthodontic tooth
movement
▫ Pressure by purulent
exudates by an acute
periradicular abscess.
Resolves once drainage for the
exudates is established.
40. Electric Pulp Test
• Stimulate the alpha δ
sensory fibers within the
pulp.
• Indicates that there are vital
sensory fibers present in at
least in part of the pulp.
• It fails to provide
information about the
vascular supply to the pulp.
• Unreliable on immature
teeth
41. Electric Pulp Test
• The presence of a response
usually indicates vital
tissue whereas the absence
of such a response usually
indicates pulpal necrosis.
• May produce false
positives or false negative
• Interpretation, comparison
and correlation with other
findings and tests must be
done.
42. Periodontal Probing
• Bone and periodontal soft
tissue destruction are
induced by both
periodontal disease and
periradicular lesions and
may not be easily detected
or differentiated
radiographically.
43. Periodontal Probing
• Probing is a diagnostic aid
that has prognostic value.
▫ Prognosis of a tooth with a
necrotic pulp that induces
cervical extending periapical
inflammation is good after
adequate root canal treatment.
▫ Outcome of root canal treatment
on a tooth with severe
periodontal disease usually
depends on the success of
periodontal treatment.
47. Normal Pulp
• Asymptomatic
• Mild to moderate transient response to thermal
and electrical stimuli that subsides almost
immediately after stimulus is removed.
• No painful response to percussion or
palpation.
• No evidence of root resorption,
• Lamina dura is intact.
• In the absence of other signs and
symptoms, teeth with canal calcifications are
considered within normal limits.
48. Reversible Pulpitis
• Thermal stimuli cause a quick, sharp,
hypersensitive response that subsides as soon
as the stimuli is removed.
• Responsive to electrical stimulation.
• No painful response to percussion or
palpation.
• Asymptomatic
• It is not a disease, it is a symptom.
• Resolves if the cause is removed
• Does not involve a complaint of spontaneous
(unprovoked) pain.
49. Reversible Pulpitis: Treatment
• The irritant should be
removed and further insult
should be prevented by
sealing the dentinal
tubules.
• If caries is diagnosed, the
tooth should be properly
restored.
• Treatment
▫ Pulp Capping
Indirect
Direct
▫ Pulpotomy
50. Irreversible Pulpitis
• Pulp is damage beyond repair.
• Severe inflammation in the pulp tissue.
• Will not resolve if the cause is removed.
• Pulp incapable to heal.
• Progress to necrosis if untreated.
• Symptomatic.
• Asymptomatic.
▫ Hyperplasic pulpitis (pulp polyp)
▫ Internal Resorption
51. Symptomatic Irreversible Pulpitis
• Pain
▫ Spontaneous
▫ Intermittent or continuous
▫ Moderate to Severe
▫ Referred Pain
▫ Provoked
• Occasionally patients may report that a
postural change induces pain.
▫ For example: Patient wakes up at night with pain
• The pain may be relieved by application of
cold.
▫ Indicates that is becoming increasingly necrotic.
52. Symptomatic Irreversible Pulpitis
• Thermal tests
▫ Lingering painful response
• Vitality test
▫ Pulp is still responsive to electrical stimulation.
• Radiographic
▫ No periapical changes
▫ Thickening of PDL
• Normal/ Positive to percussion and
palpation
• Treatment: Root Canal Treatment
53. Asymptomatic Irreversible Pulpitis
• Deep caries or restorations
• Trauma
• Slight or no pain
• Hyperplasic pulpitis (pulp
polyp)
• Internal Resorption
• Treatment: Root Canal
Therapy
54. Internal Resorption
▫ Resorption initiated within the pulp
cavity.
▫ Accidental blow or traumatic cavity
preparation have been indicated as
possible causes.
▫ It is often symmetric and exhibits
distortion of the canal wall.
55. Internal Resorption
• Pathologic state of the pulp
• Asymptomatic
• Vitality tests
▫ Normal
▫ Irreversible pulpitis
• Radiographic Evidence
• Once diagnosed endodontic
treatment must be performed.
56. External Resorption
▫ Resorption initiated in the
periodontium and affecting the
external or lateral surface of a tooth.
▫ Pulp inflammation begins when it
reaches the pulp.
58. Necrosis
• Death of the Dental Pulp
• Variable Symptoms
• Vitality Tests
▫ Non-responsive
▫ False positive- due to partial necrosis
• Radiographic
▫ Thickening PDL
▫ Apical lesion
• Bacterial Invasion
• Treatment: Root Canal Therapy
59. Pulpal Diagnosis Summary
Quick Sharp response Response with Non
response No lingering Lingering sensation responsive
No pain No spontaneous Spontaneous pain Pain/No Pain
pain
Irreversible
Normal Reversible Pulpitis
Pulp Pulpitis Symptomatic Necrotic
Asymptomatic
60. Symptomatic (Acute) Apical
Periodontitis
• Pain
▫ Moderate to severe
▫ Biting
• Vitality test
▫ Pulpitis: sensitive to cold, + to EPT
▫ Necrosis: non-responsive to cold and EPT
• Positive to percussion and palpation.
• Radiographic:
▫ Thickening of the PDL
61. Symptomatic (Acute) Apical
Periodontitis
• Treatment:
▫ Normal/ Reversible Pulpitis
Occlusal adjustment
▫ Irreversibly inflamed or necrotic pulp
Root canal treatment
▫ Other causes
Remove irritants if possible.
▫ Adjustment of occlusion and prescription of
anti-inflammatory agent (if patient is not
allergic to aspirin) must be necessary.
63. Acute Apical Abscess
(Acute Periradicular Abscess)
• Clinically
▫ Rapid onset of slight to severe
swelling
▫ Moderate to severe pain
▫ Pain to percussion and palpation
▫ Slight increase in tooth mobility
• Vitality test
▫ No response to EPT or thermal
stimulation: Necrosis
• Systemic manifestations such as
fever and general malaise.
• Radiographically:
▫ Thickening of PDL
▫ Apical lesion
64. Acute Apical Abscess
(Acute Periradicular Abscess)
• Treatment
▫ Removal of irritants by canal
debridement.
▫ Drainage through soft tissue.
▫ Teeth should not be left open to drain.
▫ Systemic antibiotic
Generally, the use of antibiotics alone
(without concurrent attempts to establish
drainage and clean the pulpal space) is not
considered an appropriate treatment.
▫ After the swelling subsides, root canal
treatment or extraction is indicated.
65. Chronic Apical Abscess
(Chronic Periradicular Abscess)
• Pain
▫ Asymptomatic
▫ Slight percussion and palpation
• Vitality test
▫ No response to EPT or thermal
stimulation: Necrosis
• Radiographically:
▫ Thickening of PDL
▫ Apical lesion
• Sinus tract
• Isolated probing to the apex
67. Condensing Osteitis
• Increase in trabecular bone in
response to persistent irritation
• Variety of Signs and Symptoms
• Vitality Tests
▫ Normal to non-responsive
• Percussion and palpation
▫ May or may not be sensitive
• Radiographic
▫ Radiopacity at the apex
Condensing osteitis
68. Differential Diagnosis for
Periapical Radiolucencies
Anatomical landmarks
Vitality tests should be done and teeth involved
should test vital. NO treatment needed.
Maxillary sinus
Mental Foramen
69. Differential Diagnosis for Periapical
Radiolucencies: Cysts
Teeth tested vital. Cases referred to
maxillofacial and oral surgeon for treatment.
70. Differential Diagnosis for Periapical
Radiolucencies
Cementoma or Cemental Dysplasia
Osteolytic stage Mature lesion
(radiolucent) (radiopaque)
Vitality tests should be done. Teeth involved
should test vital. NO treatment needed.
71. Endodontic Emergencies: Definitions
• An emergency is a severe problem
requiring an unscheduled
appointment with diagnosis and
treatment now.
• An urgency is a less severe problem
that can be attended during a
scheduled appointment.
• A rule of the true emergency is: one
tooth is the offender, i.e. the source of
pain.
72. Management of Painful
Irreversible Pulpitis
• Pain is the result of inflammation primarily in the
coronal pulp.
• Removal of the inflamed tissue will usually
reduce pain.
Complete cleaning and shaping
With limited time:
pulpal tissue should be extirpated
pulpotomy is usually effective in molars
Mild analgesics may be prescribed
Antibiotics are not indicated. with sodium hypochlorite.
Always irrigate
73. Management of Pulpal Necrosis
• Pain is related to periradicular inflammation
which results from potent irritants in the
necrotic tissue in the pulp space.
• Treatment is directed to remove or reduce pulp
irritants and the relieve of apical fluid pressure.
• With pain and pulp necrosis there may be:
No swelling
Localized swelling
Diffuse swelling
74. Management of Pulpal Necrosis
• Pulpal Necrosis without swelling
▫ The aim is to reduce canal irritants and to try to
encourage some drainage through the tooth.
Complete canal debridement after working length
determination.
If time is limited, partial debridement at the estimated
working length.
Fill canal with calcium hydroxide paste if possible; seal with
cotton pellet and temporary filling.
Prescribe analgesics
Antibiotics are not indicated.
Always irrigate with sodium hypochlorite.
75. Fascias Space Infections
• If the reaction to the infection occurs
very quickly, the involved tooth may or
may not show radiographic evidence.
• In most cases, treatment involves
incision and root canal treatment of the
involved tooth to remove the source of
infection.
• Antibiotic therapy may be indicated.
• Fascias space infections of odontogenic
origin are infections that have spread
into the fascial spaces from the
periapical area of the tooth and may
become life threatening.
76. Fascias Space Infections
• Some fascias space infections may
become life threatening cellulitis.
• If the submental, sublingual, and
submandibular spaces are involved
at the same time, a diagnosis of
Ludwig´s Angina is made
▫ This cellulitis can advance into the
pharyngeal and cervical spaces
resulting in an airway obstruction.
77. Fascias Space Infections
• Spread of infections
from the maxillary
canine or buccal spaces
can be very dangerous
because they can result
in Cavernous Sinus
Thrombosis.
▫ Life threatening
infections in which a
thrombus form in the
cavernous sinus breaks
free, resulting in a
blockage of an artery or Canine space abscess
spread of infection. spreading into the periorbital
spaces
78. Fascias Space Infections
• These are infections that have spread into the
fascias spaces from the periapical area of the
tooth.
• Swelling may be localized to the vestibule or
extend into a fascial space.
• Mild to severe pain may be present and the
patient may exhibit systemic manifestations.
79. Management of Pulpal Necrosis
• Pulp necrosis with localized swelling
▫ Abscess has now invaded regional soft tissues and, at
times, there is purulence in the canal.
Complete debridement of root canal
Fill canal with calcium hydroxide paste
Seal with cotton pellet and temporary filling.
Tissue drainage
relieve of pressure and pain
removal of a very potent irritant (purulence).
Prescribe analgesics.
Patient seldom has elevated temperature or other systemic
signs so antibiotics may not be necessary.
Always irrigate with sodium hypochlorite.
80. Management of Pulpal Necrosis
• Pulp necrosis with diffuse swelling
▫ These rapidly progressive and spreading swellings
are not localized and may have dissected into the
fasciae spaces.
▫ These patients occasionally have systemic signs.
Most important is the removal of the irritant by canal
debridement or by extraction.
Fill canal with calcium hydroxide paste
Seal with cotton pellet and temporary filling.
Incision of swelling
Rubber dam drain inserted in incision may be necessary.
Diffuse swelling decreases slowly over a period of three or
four days.
Prescribe analgesics and antibiotics.
Always irrigate with sodium hypochlorite.
81. Management of Abscesses and
Cellulitis
• Biomechanical
debridement root canals
• Incision for drainage
• Prescription of antibiotics
• Endodontic treatment
should be completed as
soon as possible.
82. Antibiotics for Endodontic Infections
• Typical regiment to treat an endodontic infections is
from 6 to 10 days on and around the clock schedule.
▫ Improvement should be seen in 24 to 48 hours after
initial treatment and initiation of the prescription.
• Penicillin VK
▫ Antibiotic of choice for treatment of endodontic
infections.
▫ High efficacy and low toxicity
▫ Spectrum includes many of the bacteria most often
identified from endodontic infections (facultative
and anaerobic bacteria).
▫ Loading dose of 1,000 mg followed by 500 mg
every six hours for 6 to 10 days.
83. Antibiotics for Endodontic Infections
• Amoxicillin
▫ Broader spectrum of activity than Penicillin VK.
▫ Absorb more rapidly and gives a higher and
more sustained serum level.
▫ Selects for more resistant organisms.
▫ Loading dose of 1,000 mg followed by 500 mg
every 8 hours for 6 to 10 days.
84. Antibiotics for Endodontic Infections
• Clindamycin
▫ Recommended for patients with a serious
infection and an allergy to penicillin.
▫ Effective against both facultative and strict
anaerobes.
▫ Although antibiotic-associated colitis has been
linked to clindamycin, it only rarely occurs in
the doses recommended for endodontic
infections.
▫ 300 mg loading dose followed by 150 to 300
mg every 6 hours for 6 to 10 days.
85. Access Preparation
• The objective of the entry is to give direct access to the
apical foramina.
• Study thoroughly diagnostic radiographs.
• The likely interior anatomy of the tooth under
treatment must be determined.
• Endodontic entries are prepared through the occlusal
in posterior teeth or the lingual in anterior teeth –
never through the proximal or gingival surface.
• Caries, defective restorations and weak structure
should be removed before starting the access
preparation.
86. Anterior Teeth
• Preparation relates to internal anatomy
• Lingual surface in the middle third of
the crown.
• Centrals and laterals: triangular shaped
with base towards incisal .
▫ Max. Laterals: curvature in about 70%
▫ Mand. Incisors: two canals: 41.4%
• Canines: ovoid
▫ Max. Canines:
Longest tooth in the dental arch
Apex often curves in the last 2-3 mm: 60%
87. Premolars
• Access shape is ovoid
extended more bucco-
lingually than mesio-
distally.
• First maxillary premolars
▫ Two canals: 85%
▫ Three canals : 6%
• Mandibular premolars
▫ One canal: 75%
▫ As a group can be the most
difficult cases to treat
endodontically.
88. Maxillary First Molar
• Largest tooth in volume and
the most complex in root and
canal anatomy.
• Is the posterior tooth with Second MB
the highest rate in failures in canal
RCT.
• Access opening shape is
triangular with the apex
towards the lingual leaving
the transversal ridge intact.
• Usually has three roots:
mesio-buccal, disto-buccal
and lingual.
89. Maxillary First Molar
• Mesio-buccal root:
▫ Most difficult root
▫ Should always be assumed
that has two canals until Second MB
canal
proven there is only one
▫ The second canal is
usually localized lingual
to the mesio-buccal canal
90. Mandibular First Molar
• Access is triangular to rhomboid in shape
with the apex to the distal and the base to
the mesial.
• Three or four canals in 93% of cases: two
mesial canals and one or two canals in
distal.
91. Second and Third Molars
• Access preparation similar to first molars.
• Maxillary molars:
▫ Access opening shape is triangular with the apex
towards the lingual leaving the transversal ridge
intact.
• Mandibular molars:
▫ Access is triangular to rhomboid in shape with the
apex to the distal and the base to the mesial.
• Third molars:
▫ Access preparation dictated by internal anatomy.
92. Instrumentation
• Main Objectives ▫ Biologic
▫ Mechanic To free the root
canal system from
To remove
pulp, bacteria and
restrictive dentin
their endotoxins.
and shape the
canal for
obturation in
three dimensions.
93. Mechanical Objectives
• Continuously tapering
preparation
• Original anatomy maintained
▫ Retained pre-operative shape
▫ Over instrumentation, failure
to pre- curve instruments and
disregarding the pass of the
guide file produce a
preparation that does not
follow the original canal
anatomy.
94. National and International Standards
for Instrumentation
• The cross section at the first rake angle is term D0.
• D16 is the area of the largest diameter 16 mm coronally to
D0.
• Standardized instruments have a taper of 0.32 mm from
D0 to D16, e.g. file #10 has a D16 of 0.42 mm.
95. National and International Standards
for Instrumentation
• Files #10 through #60 have diameters of D0 that
increases by 0.05 mm.
• From file #60 to #140 the D0 increases by 0.10 mm.
• D0 corresponds to the number of the file in tenths of
mm, e.g. file #10 is 0.10 mm in diameter at its D0.
96. Sodium Hypochlorite (NaOCl)
• Is an excellent antimicrobial agent.
• Is a powerful and inexpensive irrigant
• Dissolve pulp tissue.
• Lubricates canal facilitating instrumentation.
• Used clinically in concentrations of 3 to 5%.
97. Chelating Agents
• The purposes of the chelator are:
▫ lubrication
▫ emulsification
▫ holding debris in suspension
• Chelating agents may be used clinically to
facilitate cleaning and shaping.
• In calcified canals EDTA (ethylene-
diaminetetracitic acid) soften dentin and
minimize blockages.
• RC-Prep or ProLube are chelators in a viscous
suspension.
98. Calcium Hydroxide
• Intra-canal medicament most recommended and
used.
• Powerful alkaline (pH approximately 12.5)
• It is a slowly working antiseptic.
• Kills bacteria in the root canal space
• Controlled laboratory studies support the use of
calcium hydroxide as an antimicrobial agent before
obturation of teeth with pulp necrosis.
99. Obturation Objective
• To create a complete
seal along the length
of the root canal
system from the
coronal opening to
the apical
termination.
Pre-treatment Post-treatment
100. Obturation Objective
• Eliminate all
avenues of leakage
from the oral cavity
or the periradicular
tissues into the root
canal system.
Pre-treatment Post-treatment
101. Obturation Objective
• Seal within the system
any irritants that can
not be fully removed
during canal
instrumentation.
Pre-treatment Post-treatment
102. Coronal Restoration
• After canal
obturation, coronal
seal (with a proper Recurrent caries
restoration) is of due to poor
marginal seal
ultimate importance.
• Coronal leakage due
to improper coronal
restoration is the
most common cause Leaking
of failure in root canal temporary
treatment. restoration
103. Procedural Accidents
• Perforations during access preparation
• Accidents during cleaning and shaping
• Accidents during Obturation
• Accidents during pos space preparation
104. Perforations
• During access preparation
• Lateral root perforation at or above the height
of the crestal bone
• Lateral root perforation below crestal bone
• Furcation perforation
105. Perforations
Lateral
▫ Prognosis for perforation repair is favorable.
▫ These defects can be easily repaired with
standard restorative materials such as
amalgam, glass ionomer or composite.
In some cases the best repair is placement
of a full crown with the margin extended
apically to cover the defect.
106. Lateral root perforation below crestal
bone
• These perforations generally have the poorest
prognosis.
▫ Attachment often recedes and a periodontal pocket
forms.
• Treatment goal is to position the apical portion of
the defect above the crestal bone.
▫ Orthodontic root extrusion is the procedure of choice
▫ Crown lengthening may be considered
• Internal repair of these perforations by mineral
trioxide aggregate (MTA) has been shown to
provide an excellent seal as compared to other
materials.
107. Furcation Perforation
▫ A direct perforation usually occurs during a
search for a canal orifice.
▫ Should be immediately repaired with MTA or, if
proper condition exists (dryness), glass ionomer
or composite in an attempt to seal the defect.
Prognosis is usually good if the defect is sealed
immediately.
108. Furcation Perforation
• Surgical Treatment
▫ Surgery requires more complex
restorative procedures and more
demanding oral hygiene from the
patient.
▫ Surgical alternatives are
hemisection, bicuspidization, root
amputation and intentional
replantation.
109. Ledge or Block Formation
Prognosis
• Depends on the amount of debris left in the
uninstrumented and unfilled portion of the
canal.
• Patient must be informed about the
prognosis, the importance of the recall
examination and which signs indicate failure.
• Appearance of clinical symptoms or
radiographic evidence of failure may require
referral for apical surgery or retreatment
110. Root Perforations
• Roots may be perforated at different levels during
cleaning and shaping.
• Location of the perforation affects the prognosis.
▫ Repair of stripping perforation in the coronal third of the
root have the poorest long term prognosis.
• The periodontal response to the injury is affected
by the level and size of the perforation.
• Perforations in the early stages of cleaning and
shaping that leave undebrided portions of the
canal(s) have a poorer prognosis that those where
the canal(s) are thoroughly clean.
111. Separated Instruments
• Imperative to inform the patient
• Attempt to remove the instrument
• Attempt to by-pass the separated instrument using a
small file.
• If the instrument cannot be by-passed, preparation and
obturation should be done up to the fragment.
• If symptoms appear, a periapical surgery or extraction
are the options.
• A separated instrument, per se, does not lead to a
failure of endodontic therapy. However, may lead to a
treatment failure if it obstructed proper debridement of
the root canal space.
113. Cracked Tooth Syndrome
• Hairline, incomplete fracture
of a vital tooth.
• The fracture involves enamel
and dentin and sometimes
involves the dental pulp.
• Most cracks run mesio-distally
and are rarely detected
radiographically when are
incomplete.
114. Cracked Tooth Syndrome
• Chief complaint:
▫ Sporadic sharp pain
▫ Pain on chewing,
▫ Occasional pain from
cold.
• Unable to locate the
source of pain.
• Asymptomatic.
115. Diagnosis
Tooth Slooth
Transillumination Methylene Blue
117. Prognosis
• The apical extension and
future migration of the defect
down onto the root will decide
the outcome.
• The prognosis for a vertical
root fracture extending
apically from the alveolar crest
is poor, and tooth extraction is
often indicated.
118. Vertical Root Fracture
• Indicators
▫ Narrow periodontal pocket
▫ Sinus tract
▫ Lateral radiolucency extending to the
apical portion of the vertical fracture.
▫ The fracture is rarely visible on
radiographs
• Prognosis and Treatment
▫ Poorest prognosis of all procedural
accidents
▫ Treatment is removal of the involved
root in multirooted teeth or extraction.
119. Vertical Root Fracture
Etiology
• Excessive instrumentation
• Excess force during compaction of root filling
material
• Widening of canal during post space
preparation
• Unfavorable post length
120. Endodontic Failures
• Can be attributable to inadequacies in:
▫ Cleaning
▫ Shaping
▫ Obturation
▫ Iatrogenic events
▫ Re-infection of the root canal system when the coronal
seal is lost
• Regardless of the initial cause, the sum of all
causes is leakage.
121. Surgical or Nonsurgical?
• Nonsurgical retreatment (NSRCT) is an
endodontic procedure used to
▫ remove materials from the root canal space
▫ address deficiencies
▫ repair defects that are pathologic or iatrogenic
• Nonsurgical endodontic retreatment efforts are
directed toward eliminating microleakage.
122. Surgical or Nonsurgical?
• In NRSCT, endodontic failures are evaluated for
▫ coronal leakage
▫ fractures
▫ missed canals
• Pathologic and iatrogenic events can be repaired
non- surgically.
123. Periradicular Surgery
Procedure
To remove a portion of the root with undebrided canal
space or to retro seal the canal when a complete seal can
not be obtained with conventional endodontics.
124. Periradicular Surgery
• Indications
▫ NSRCT is not feasible
▫ Failure of a NSRCT
▫ Retreatment will not produce a better result
▫ Biopsy is indicated
▫ Persistent periapical pathosis
▫ Periapical lesion that enlarges after NSRCT
▫ Overextension of obturation material interfering
with healing
▫ Apical portion of the root with apical lesion
cannot be cleaned, shaped, and obturated.
125. Periradicular Surgery
• Contraindications
▫ Treatment of choice is NSRCT
▫ Unidentified cause of treatment failure
▫ Anatomic Factors
Inaccessibility to the surgical site
Spaces such as maxillary sinus or proximity
of neurovascular bundles
126. Periradicular Surgery
Sequence of Procedures
• Flap design • Root-end filling
• Incision and reflection ▫ MTA (Pro Root)
• Apical access • Flap replacement and suturing
• Periradicular curettage • Post-operative care and
• Root-end resection instructions
• Root-end cavity preparation • Suture removal and evaluation
▫ Ultrasonic instruments offer
advantages of control and
ease of use and permits less
apical root beveling and
uniform depth of
preparation.
127. Vital Pulp Therapy
• Treatment to maintain and preserve the vitality
of the tooth.
• Highly recommended in teeth with incomplete
formed roots and young teeth.
129. Open Apex
• The developing root of Open Apex
immature teeth until apical
closure occurs.
• Apex closes approximately 3
years after eruption.
Thin Walls
130. Open Apex
• These teeth are difficult to Open Apex
treat.
• Difficulties:
▫ The canal is wider apically
than coronally
▫ A modified access is needed.
▫ The canal walls are thin and
susceptible to fracture.
• Long-term prognosis is
questionable. Thin Walls
131. Apexogenesis
• A vital pulp therapy
procedure performed to
enable continued
physiological development
and formation of the root
end.
Calcium
Hydroxide/MTA
132. Apexogenesis
• A vital pulp therapy procedure
performed to enable continued
physiological development and
formation of the root end.
• In young teeth it allows root
formation and dentin
deposition to have a good Calcium
crown–root ratio and an Hydroxide/MTA
adequate thickness of the root
in order to avoid possible root
fractures.
133. Apexification
• A method to induce a
calcified or artificial barrier
in a root with an open apex
or the continued apical
development of an
incompletely formed root in Calcium
Hydroxide/
MTA
teeth with necrotic pulps.
134. Pulp Therapy
• The stage of development influences the type of
pulp therapy rendered when pulp injury occurs.
135. Vital Pulp Therapy: Requirements
• Treatment of a non
inflamed pulp
• Proper Diagnosis
• Clinical Judgment
Histologic appearance of the pulp within 24
hours of a traumatic exposure. There is
approximately 1.5 mm of inflamed pulp below
the surface of the fracture.
136. Vital Pulp Therapy
Indications
• Trauma
• Some mature teeth
• RCT and subsequent
restoration not affordable
• Teeth with calcification of the
pulp chamber and canals are
not candidates
• Bacteria tight seal
▫ Most critical factor for a successful
treatment
139. Vital Pulp Therapy
Pulp capping
Indirect
Procedure in which a material is placed on a thin
partition of remaining carious dentin that if
removed might expose the pulp.
Step-Wise Excavation of Caries.
140. Vital Pulp Therapy
Pulp Capping
Indirect
Treatment to avoid pulp exposure.
Promote dentinal sclerosis.
Stimulate reparative dentin.
Allows the pulp to protects itself against caries.
141. Indirect Pulp Capping
Indications
• None or minimal pulpal
inflammation.
▫ Vital tooth.
▫ No spontaneous pain.
▫ No periapical pathology.
• Deep carious lesion that
will expose pulp if
removed completely.
142. Indirect Pulp Capping
Follow -Up
• Reevaluate in 6 to 8
weeks.
• Check of pulpal status
• Remove remaining
caries using rubber
dam.
• Restore permanently.
143. Vital Pulp Therapy
Pulp capping
Direct
Treatment of an exposed vital pulp by sealing the
pulpal wound a with a dental material placed in direct
contact with the exposure to facilitate the formation of
reparative dentin and maintenance of the vital pulp.
144. Direct Pulp Capping
Indications
Mechanical and traumatic exposures
▫ Immature permanent teeth.
▫ Mature permanent teeth with a simple restorative
plan.
None or minimal pulpal inflammation
▫ Normal or reversible pulpitis.
▫ Asymptomatic
▫ No periapical pathology.
145. Direct Pulp Capping
• Dressing directly on pulp exposure.
• Mechanical exposures have better prognosis
than carious exposures.
• If the exposure is on the axial wall, a pulpotomy
or pulpectomy should be performed rather than
a pulp cap.
• In caries, the larger the exposure, the poorer the
prognosis.
• On trauma, the size of the exposure does not
influence healing.
146. Direct Pulp Capping
Follow-up
• Vitality testing at 3 weeks, 3, 6, and 12 months
and yearly thereafter
• Radiographic examination
• Prognosis: success in the 80% range
147. Partial Pulpotomy
(Cvek Pulpotomy)
• Differs from pulp capping in that a portion of
the remaining pulp is removed.
• Indications are similar to pulp capping.
• Inflammation zone has extended more than
two millimeters apically from exposition.
• Success rate is 94 to 96%.
148. Partial Pulpotomy
(Cvek Pulpotomy)
• Indications are similar to pulp capping
• Inflammation zone has extended more than two
millimeters apically from exposition
• Success rate is 94 to 96%
149. Successful Vital Pulp Therapy
• Non-inflamed vital pulp
• Continued apical growth
of the root with a normal
or nearly normal apex is
expected in immature
treated teeth.
• Maintenance of positive
sensitive tests
150. Treatment Failure
• Cessation of growth and/or apical disease
• Inflamed pulp or necrosis
• Further treatment:
▫ Root-end closure
Apexification
MTA plug
▫ Root canal treatment
151. Open Apex
• Treatment alternatives for necrotic teeth
▫ Apexification
▫ MTA plug
▫ Revascularization
152. Open Apex
• Open apex is found:
▫ In developing roots of immature
teeth.
▫ In necrotic teeth before root
development is complete.
▫ As a result of extensive resorption of
a mature apex due to different
causes:
Orthodontic movement
Periradicular inflammation
Cysts
153. Apexification
• The process of inducing a calcified
barrier in a necrotic tooth with an
open apex.
• Indicated for immature teeth in
which standard instrumentation
techniques cannot create an apical
stop.
• Allows a calcified barrier to form
across the open apex.
• Results in blunting of the end of
the root.
154. Apexification: Procedure
The Ca(OH)2 is packed against the apical soft tissue with a plugger
to initiate hard tissue formation.
155. Apexification: Follow-up
• A radiograph is taken at 3-month intervals up to
one year to evaluate whether a hard-tissue
barrier has formed
• Successfully treated teeth are characterized by
the following:
▫ Absence of signs or symptoms of periradicular
pathosis.
▫ Presence of a calcified barrier across the apex as
demonstrated by radiographs or, more often, by
careful tactile probing with a file.
156. MTA Plug
• Clean and prepare canal.
• Calcium hydroxide left for at least two weeks.
• Remove Ca(OH)2.
• MTA is carried into the canal.
• Create a 3 to 4 mm apical plug.
• In a subsequent appointment, obturate canal
with gutta-percha
• Final restoration.
157. MTA Barrier
The mix is condensed to
the apical extend using
pluggers or paper points
to create a 3 to 4 mm
apical plug.
MTA placed
In a subsequent appointment, the
remainder of the canal is obturated
with gutta percha and a final restoration
is placed.
158. Revascularization
• Technique to treat immature
teeth with apical periodontitis.
• Canal disinfected
• Mix of antibiotics
• Apex irritated-blood clot
• Coronal tight seal
159. Treatment Summary
Reversible Irreversible pulpitis
pulpitis Necrotic pulp
Vital Pulp therapy Closed apex Open apex
Pulp capping or
pulpotomy Root Canal Root end closure:
Therapy CaOH2
MTA plug.
Revascularization
160. Definition of a Perio-Endo Lesion
▫ At least one necrotic, not simply irreversible
inflamed, canal is to be expected when a
moderate to large periapical lesion is
present.
▫ There must be a periodontal defect that can
be probed to either the apex of the tooth or
to the area of an involved lateral canal.
• Both root canal therapy and periodontal
treatment are required to resolve the
entirety of the lesion.
161. Primary Endodontic Lesions
• Endodontic lesions resorb bone
apically, laterally, and destroy the
attachment apparatus adjacent to a
non vital tooth.
• Inflammatory process in the
periodontium occurring as a result
of root canal infection may not only
be localized at the apex, but may
also appear along the lateral aspect
of the root and in furcation areas of
two and three-rooted teeth.
162. Primary Endodontic Lesions
• Because this lesion is an
endodontic problem that has
merely fistulated through the
periodontal ligament, complete
resolution is usually anticipated
after routine root canal
treatment.
163. Primary Periodontal Lesions
• Clinically, there is tooth mobility
• The affected tooth respond
positively to pulp testing.
• Careful periodontal examination
will usually reveal pocket
formation and an accumulation
of plaque and calculus.
• Prognosis depends exclusively
on the outcome of periodontal
therapy.
164. Perio-Endo: Treatment Decision
Conical with narrow
probing at base of defect
True Combined Perio-Endo Lesion
Given: bone loss Conical Pulpless tooth with separate
from the CEJ to or Non periodontal defect
near the apex Vital WNL
Probing Endo only
Single
Endo only
Pulp Narrow Endo only
Radiograph
Tests Possible vertical Fracture
Multiple/Conical
Perio only
WNL
Vital Probing Pathosis; possible biopsy
Narrow
Exceptions:
Enamel spurs
Developmental grooves
Defect after trauma
165. Restoration of Endodontically Treated
Anterior Teeth
• Intact, non vital anterior teeth that have no loss
of tooth structure beyond the endodontic access
are at minimal risk of fracture and do not
require a crown.
• A non vital anterior tooth that has lost
significant tooth structure requires a crown.
• Placement of dowel and core depends on the
amount of remaining tooth structure.
166. Restoration of Endodontically Treated
Posterior Teeth
• Restoration must be planned to protect posterior
teeth against fracture.
• The functional forces against molars require
crown or onlay protection.
• Placement of dowels (posts) and core depends
in the amount of remaining tooth structure.
• When there is sufficient tooth structure to retain
the core and the crown, dowels are not needed.
167. Dowels (post)
• Dowel is a post or other
relatively rigid, restorative
material placed in the root of a
non vital tooth. CROWN
• Purpose of the dowel is to CORE
provide retention for the core
and coronal restoration.
• Dowel does not strengthen the DOWEL
tooth and is not necessary when (POST)
substantial tooth structure is
present.
• Tooth is weakened if dentin is
sacrificed to place a large Gutta
diameter dowel. Percha
168. Conventional Dowels
• Always use RD during post
preparation. CROWN
• Passive CORE
• Cemented into place
• Residual dentin should DOWEL
undergo minimal alteration (POST)
• Length and diameter should
be the minimum dimension
needed to withstand functional
loading.
▫ At least 5 mm of filling material should
be left at apex.
169. Coronal Coverage
• Coronal restorations reestablish function and
prevent microleakage.
• As a general rule, endodontically treated
posterior teeth and anterior teeth where
extensive tooth structure is missing and
integrity, function and esthetics must be
restored, should be restored with coronal
coverage.
• Crowns should restore function without
harm to the remaining root or the periodontal
attachment.
170. Ferrule Effect
FERRULE
• Ideal characteristics:
▫ Minimum of 2 mm in
2 mm
height
▫ Parallel axial walls
▫ Completely encircle the
tooth
▫ End on tooth structure
▫ Not invade the attachment
apparatus of the tooth
171. Standards of Success
• The patient should be asymptomatic and able
to function equally well on both sides.
• The periodontium should be healthy
including a normal attachment apparatus.
• Radiographs should demonstrate healing or
progressive bone fill over time.
• The principles of restorative excellence
should be satisfied.
The inherent healing potential of the dental pulp is well recognized.Unlike most tissues, the pulp has essentially no collateral circulation; for this reason, it is theoretically more vulnerable than most other tissues. In the case of severe injury, healing would be impaired in teeth with a limited blood supply. It seems reasonable to assume that the highly cellular pulp of a young tooth, with a wide-open apical foramen and rich blood supply, has a much better healing potential than an older tooth with a narrow foramen and a restricted blood supply.
The inherent healing potential of the dental pulp is well recognized.Unlike most tissues, the pulp has essentially no collateral circulation; for this reason, it is theoretically more vulnerable than most other tissues. In the case of severe injury, healing would be impaired in teeth with a limited blood supply. It seems reasonable to assume that the highly cellular pulp of a young tooth, with a wide-open apical foramen and rich blood supply, has a much better healing potential than an older tooth with a narrow foramen and a restricted blood supply.
Tertiary dentin has been suggested to be secreted by original odontoblasts or in case of their death, by newly differentiated replacement odontoblasts originating from nearby mesenchymal stem cells. The function of the tertiary dentin is to protect the pulp from noxious influences. Tertiary dentin is disorganized in structure compared to primary and secondary dentin.The first layer of the primary dentin to be deposited is mantle dentin. It is produced by odontoblasts that are not yet fully differentiated. In the adult tooth, mantle dentin is the oldest dentin and is produced adjacent to the enamel in the crown.Predentin is a 15- to 20-µm unmineralized organic matrix layer of dentin situated between the odontoblast layer and the mineralized dentin.A characteristic of human dentin is the presence of tubules that occupy from 1% (superficial dentin) to 30% (deep dentin) of the volume of intact dentin.[107],[277] The diameter of tubules vary from 1 µ to 2.5 µm and traverse the entire thickness of dentin from the DEJ or CDJ to the pulp. They are slightly tapered, with the wider portion situated toward the pulp.
Nos indica el grado de integridad de los tejidos de soporte del diente.
Ayuda en la prognosis Diente vital con bolsillos Dinete necrotico con bolsillo
La infeccion se puede regar y alojarce en diferentes espacios faciales . La severidad va a depender q haya o no manifestaciones sistemicas de la condicion
Therefore its is important in order to achieve predictable results, the clinician must have knowledge of apical anatomy, able to interpret radiographs and be able to correctly use an electronic apex locator